Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One prediction of the protease-antiprotease hypothesis of chronic obstructive pulmonary disease (COPD) pathogenesis is the appearance of elastin-derived degradation products in the plasmas of affected patients that are due to the breakdown of alveolar interstitial elastin by an excess of elastolytic activity in the lung. We previously demonstrated a significant elevation of plasma elastin-derived peptides (EDP) in subjects with COPD in comparison with asymptomatic smokers with normal spirometry or normal nonsmokers. To better determine the selectivity of the assay for EDP as a marker of COPD, we measured plasma EDP levels in different patient populations. These included subjects with COPD, subjects with diseases that may involve accelerated elastolysis (pneumonia, atherosclerotic vascular disease, and inflammatory arthritis), subjects with diseases hypothesized to involve pulmonary inflammation without elastolysis (asthma and acute tracheobronchitis), asymptomatic smokers with normal spirometry, and healthy, nonsmoking subjects. Mean plasma EDP levels in subjects with COPD were elevated above those in all other subjects (p less than 0.01). The prospective analyses of specificity and sensitivity of plasma EDP levels as markers of COPD gave values of 91 and 65%, respectively. Utilizing receiver operating characteristic curve analysis to assess the diagnostic and screening performance of plasma EDP as a test for COPD (perfect test equals an area under the curve of 1.0), the area under the curve was 0.87, which compares favorably with many widely used clinical tests. These data demonstrate that the assay for plasma EDP is a quantitative, easily measured, and highly specific marker for subjects with COPD.
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PMID:Specificity and sensitivity of the assay for elastin-derived peptides in chronic obstructive pulmonary disease. 846 8

In order to evaluate the risk for proteolytic destruction of lung parenchymal elastic fibers in ventilated premature infants, the concentrations of elastase were determined in tracheal aspirates of 65 infants from whom we obtained a total of 327 sequential samples. Elastase was detected at least once in 39 of the 65 infants studied. Eleven of these infants were ventilated with greater than 60% oxygen for greater than 5 days. In 19 infants, the presence of elastase was associated with positive bacterial and/or viral cultures and/or elevated ratios (greater than 0.22) of immature neutrophils to total neutrophils. Elastase was not detected in the lung secretions of 26 infants ventilated with greater than 60% oxygen for less than 3 days, suggesting minimal risk for elastic fiber destruction in the intubated infant who neither has pneumonia nor requires prolonged hyperoxic ventilation. The risk for elastic fiber destruction was further evaluated by analyzing sequential urine and tracheal aspirate samples for the presence of an elastolytic degradation product of elastin (desmosine). The biochemical data indicated a potential risk for proteolytic destruction of elastic fibers in association with infection and/or prolonged hyperoxic exposure. In addition, autopsy specimens obtained from three of the infants revealed structurally abnormal lung parenchymal elastic fibers. Because elastic fibers are believed to provide the structural support for alveolar septal development, proteolytic degradation of these fibers may be a significant factor in the impaired lung development that occurs in infants with bronchopulmonary dysplasia.
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PMID:Risk factors for the degradation of lung elastic fibers in the ventilated neonate. Implications for impaired lung development in bronchopulmonary dysplasia. 162 5

This article reviews the medical literature concerning available diagnostic tools for managing nosocomial respiratory infections in mechanically ventilated patients. The first part deals with the reliability of the clinical criteria used in diagnosing nosocomial pneumonia in such patients and the accuracy of simple markers of pneumonia such as elastin fibres stain and antibody-coated bacteria. The second part reviews the presently available non-invasive and invasive methods for diagnosing pulmonary infections acquired during mechanical ventilation. With regard to invasive methods, protected specimen brush and bronchoalveolar lavage are extensively discussed in view of the different results in the literature. At the present time, these two methods seem to be the most accurate techniques available. The fact that bronchoalveolar lavage may combine the cytological examination and the quantitative culture of the sample obtained is noted. The role of percutaneous lung needle aspiration is also mentioned. Finally, histological diagnosis of pneumonia and pulmonary postmortem biopsy cultures are reviewed as "gold-standard" reference methods for investigation in this field. Future directions for further clinical research are addressed.
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PMID:Accuracy of diagnostic tools for the management of nosocomial respiratory infections in mechanically ventilated patients. 178 74

During staphylococcal pneumonia massive destruction of lung tissue is often observed. Staphylococcal serine proteinase (SSP) inactivates alpha-1-proteinase inhibitor (alpha 1PI) a major factor which protects lungs from phagocyte proteases. We investigated the effect of SSP on elastin degradation by porcine pancreatic elastase (PE) and crude extract of human neutrophil elastase (NE) in solution and gel containing alpha 1PI. SSP having no elastase activity enhanced PE and NE-induced elastinolysis in solution when added to alpha 1PI before mixing with elastase and then with elastin. SSP added simultaneously with alpha 1PI to PE had no influence on elastin degradation. However, SSP added simultaneously, 30 min before or 30 min after PE significantly increased elastin digestion in elastin-agarose plate with alpha 1PI. Maximal increase in elastinolysis about 3-fold was for SSP added 30 min prior to PE. Since elastin is the major component of the alveolar walls it is possible that lung damage in the course of staphylococcal infection may partly depend on action of SSP.
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PMID:Serine proteinase from Staphylococcus aureus enhances elastin degradation by elastases in the presence of human alpha-1-proteinase inhibitor. 185 84

The clinical distinction between bacterial colonization of the tracheobronchial tree and nosocomial pneumonia is difficult, especially in intubated patients. We studied 51 intubated, intensive care unit patients prospectively by serial examinations of tracheal aspirates for elastin fibers, graded Gram's stains, and quantitative bacterial cultures in conjunction with clinical and radiologic observations in an attempt to develop criteria for the early detection of pulmonary infection. Patients with infection had new or progressive pulmonary infiltrates plus 1 of the following: positive blood culture results, radiographic evidence of cavitation, or histologic evidence of pneumonia, or 2 or more of the following: new fever, new leukocytosis, or grossly purulent tracheal aspirates. Twenty-one patients developed infection, 22 remained colonized, and 8 had an uncertain status. Infiltrates developed in 34 patients (21 infected, 8 colonized, 5 uncertain status). Gram-negative bacilli were most commonly isolated and were more frequent in infected patients (81 versus 47%, p less than 0.05); Pseudomonas aeruginosa and Serratia marcescens were most often associated with infection. No differences were observed between infected and colonized patients in demographic features, smoking history, underlying disease, previous antibiotic therapy, days in hospital before intubation, preexisting pneumonia upon intubation, or highest temperature or leukocyte count during course. By univariate analysis, infected patients had a longer duration of intubation (p less than 0.05), higher Gram's stain grading for neutrophils (p less than 0.05) or bacteria (p less than 0.005), higher bacterial colony counts (p less than 0.05), and more frequent detection of elastin fibers in tracheal aspirates (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnosis of nosocomial pneumonia in intubated, intensive care unit patients. 310 59

Altogether 274 patients with different pulmonary diseases were examined for the activity of trypsin and elastase of the blood and the level of their inhibitors. The concentration of antibodies to collagen and elastin was also measured. In acute chronic pneumonia or exacerbation, the activity of the enzymes increased, the concentration of antibodies to collagen and elastin rose. In acute pneumonia, the titer of antibodies to collagen and elastin persisted for 1-1.5 months, in CNPD and tuberculosis for 4-8 months.
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PMID:[Protease activity and the level of antibodies to connective tissue elements in various lung diseases]. 389 Feb 58

72 cases of diffuse interstitial lung diseases were observed from 1969 to 1976. Specimens removed from 47 patients were subjected to the whole spectrum of reactions. According to variation of both elastin and collagen, the following groups were outlined: group A: mycobacteriosis, farmer's lung, sarcoidosis and silicosis; group B: chronic eosinophilic pneumonia, lymphocytic interstitial pneumonia, post-tuberculous pulmonary fibrosis, and group C: X-ray pneumopathy, desquamative interstitial pneumonia, sclerodermic pneumopathy and chronic pulmonary fibrosis (primary chronic fibroadenomyosis). Each of these groups presents a close relationship between histochemical, radiological, clinical and functional findings.
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PMID:Diffuse interstitial lung diseases: a histochemical approach. 623 29

This study examines the bronchial alveolar lavage (BAL) samples from a group of patients with acute bacterial pneumonia (n = 13) and makes a comparison with a control group (n = 5). The proteinase inhibitory capacity was examined and found to be composed primarily of alpha 1-proteinase inhibitor (PI, alpha 1-antitrypsin) and, to a lesser extent, bronchial mucosal inhibitor. Although the average PI concentration was elevated approximately 5-fold in the pneumonia group, its inhibitory function against elastase was decreased 15-fold when compared with that in the control group. The pneumonia group showed an increased concentration of immunologically identified elastin-derived peptides. Some of the BAL fluid from patients with pneumonia showed elastolytic activity against amorphous insoluble lung elastin. The majority of the elastase appears to be of neutrophil origin. Bronchial mucosal inhibitor is shown to be a component of both normal and pneumonia BAL fluids by both immunologic quantitation and by its resistance to perchloric acid inactivation. Compared with those from control subjects, BAL samples from patients with acute bacterial pneumonia showed a decreased proteinase inhibitor function and both increased elastolytic activity and elastin-derived peptide concentration.
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PMID:Proteinase inhibitory function in inflammatory lung disease. I. Acute bacterial pneumonia. 660 52

The diagnosis of nosocomial pneumonia is especially difficult in intubated patients due to the low specificity of their clinico-radiological signs. The objective of this study was to evaluate the usefulness of basing diagnosis on elastin fibers (EF) in bronchoaspirate (BAS) as an indication of pneumonia in mechanically-ventilated (MV) patients. Forty-seven MV patients suspected of having nosocomial pneumonia were studied prospectively. Fiber bronchoscopy was carried out on all patients and samples were obtained using a protected catheter brush (PCB) and bronchoalveolar lavage (BAL). A purulent sample of BAS was also examined, after addition of 40% KOH, to determine the presence of EF. EF was found in 15 patients, 11 of whom had pneumonia while 3 more had necrotizing pneumonia (sensitivity 52%, specificity 85%). Ten of the 17 microorganisms isolated in the cases of EF positive pneumonia were gram negative, although the germ found most often was S. aureus. There were no differences in the prognosis for pneumonia patients who were EF positive and those who were EF negative. In conclusion, once necrotizing pneumopathology has been ruled out, the presence of EF in BAS may offer reasonable support for firm diagnosis in some MV patients with pneumonia.
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PMID:[The usefulness of elastin fibers as a diagnostic marker in ventilator-related pneumonia]. 802 84

Captopril protects rat lung from radiation-induced pneumonitis and fibrosis and preserves function and survival in experimental radiation nephropathy. This study determined the structural benefit of captopril used preventively in radiation nephropathy. Twenty-eight Wag/RijMCW rats, divided in six groups, received 0 to 17 Gray total body irradiation followed by syngeneic bone marrow transplant. Captopril 0, 62.5, 125, 250, or 500 mg/l was given in the drinking water from the time of irradiation, and the rats were killed at 20 weeks. Using light and electron microscopy, kidneys of irradiated no-drug rats showed glomerular tuft capsular adhesions and hyalinization, focal tubular necrosis, severe interstitial fibrosis, and marked thickening and hyaline degeneration of the wall of interlobular arteries and arterioles, with intimal proliferation and periadventitial edema and inflammation. Lumens of the smaller arteries were often occluded. Significant collagen deposition was present in glomeruli, interstitium, and adventitia of interlobular arteries. Marked reduction of glomerular, tubular, vascular, and interstitial damage was seen in irradiated, captopril-treated animals, with only mild focal tubular interstitial injury and fibrosis seen. alpha smooth muscle actin-positive cells, probably myofibroblasts, were enhanced in the irradiated kidneys, and this expression was reduced in a dose-related fashion by captopril. There was also reduction in the arteriolar wall thickening, luminal occlusion, and collagen deposition in captopril-treated animals. The presence of elastin was not affected by radiation or drug treatment. Blood pressure and azotemia were lower and survival was higher in irradiated drug-treated rats compared with irradiated no-drug rats. We conclude that captopril exerts significant functional and structural protection against renal radiation injury. There was notable reduction in radiation-induced fibrosis in captopril-treated animals in this model, as in experimental lung radiation injury.
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PMID:Captopril preserves function and ultrastructure in experimental radiation nephropathy. 880 58


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